Renal pre-exam

jdlevenson's version from 2015-05-07 02:52

Lecture 22

Question Answer
C < GFRNet Reabsorption
C > GFRNet Secretion
AKI definitionRecent/ within the past month increase in Cr of at least .5-1 mg/dL over baseline or reduction of Cr clearance of 50% or more. When Cr <2, small changes indicate a significant change in GFR
Three types of intrinsic AKITubular Necrosis (Ischemia and Toxins), Interstitial
Nephritis and Acute Glomerulonephritis/ glomerular diseases.
Question Answer
Cirrhosis and CHF could lead to what type of AKIPrerenal. Also RAS or Volume depletion or Hemorrhage.
Prerenal pathophysiology, Absolute or Relative decrease in EAV leads toCentral and peripheral baroreceptors -> vasoconstriction of non vital organs -> decreased renal blood flow.
In prerenal, Angiotension II actions on kidneyIn response to decreased intravascular volume and increased renin, A2 -> efferent arteriole constriction >>> afferent arteriole constriction so that the drop in GFR is not as large as it would be otherwise. But A2 is responsible for drop in GFR.
NE actions in Proximal TubuleIncrease Sodium and Water reabsorption.
How does Urea absorption increase in prerenal AKIMore Na and Water absorption; more concentrated fluid in proximal tubule -> stronger concentration gradient for reabsorption of Urea. BUN to Cr > 20:1.
Prerenal AKI, urine sodium<20. More absorbed. However since confounded by water absorption, need to look at FENa too, which will be less than 1%.
FENa equationQuantity of sodium excreted/ filtered x 100; (Una x V) / (Pna x (Ucr x V/ Pcr)). Clearance of Sodium / Clearance of Cr x 100.
Non-pre-renal state, FeNa will be>1%
Normal urine osmolarity290.
Prerenal labsSerum BUN: Cr >20:1; Urine Na <20; FENa <1%; Urine osmolarity >500 mOsm/kg or > serum Osm.
Ineffective intravascular volume (rather than true volume depletion)Cirrhosis/ hepatorenal syndrome and CHF. Perceived hypoperfusion.
In RAS, what hormone releaseAngiotensin II, vasoconstriction to help increase blood flow to kidney; A2 constricts efferent > afferent so drop in GFR is not as large.
RAS and ACE-I and ARBsLarger drop in GFR due to loss of compensatory efferent arteriole constriction > afferent arteriole.
In prerenal, A2 and NE stimulate production ofProstaglandins – prostacyclin and PGE2. Work together with A2 and NE to prevent drastic unopposed drop in GFR. BALANCE.
NSAIDs decrease GFR in Prerenal becauseNSAIDs block prostaglandins and mess up balance between vasoconstriction and vasodilation and so GFR decreases.
Prerenal treatmentFluids (and underlying cause of hypovolemia and or hypoperfusion).
ATN common TOXIC causesIV contrast for CT scan or cardiac cath; aminoglycosides; myolobunuria from rhabdomyolysis (recall, ACE-I and Daptomycin) and hemoglobinuria from severe hemolysis (myoglobin and Hb are toxic)
Ischemic ATN happens whenProlonged prerenal states like sepsis or shock -> hypoperfusion -> tubular necrosis.
Proximal tubule vs distal tubule on histologyProximal has a brush border.
Since ATN does not affect glomerulus, there will be no change in GFRFalse. GFR decreases. Not clear explanation.
ATN dx slidesMuddy brown granular casts. Necrotic cells accumulated in tubules.
ATN dx labsBUN:Cr preserved (10:1, 15:1); Urine sodium > 20, FeNa >1% and urine osmolarity will be similar to plasma osmolarity.
RBC CastNephritic syndrome; still intrinsic AKI.
WBC CastInfection/ AIN, still intrinsic AKI.
Clinical settings of postrenal AKIBPH; prostate cancer; cervical cancer; bladder tumor; kidney stones. These may present on physical (palpable/ percussable bladder, lymphadenopathy, etc).
Postrenal AKI dx byUltrasound and then if necessary foley catheter.
Limitation of foley catheterRemove as soon as possible bc infection. ONLY RELIEVES OBSTRUCTION IF IT IS AT OR BELOW LEVEL OF BLADDER.
Post-obstructive diuresisObstruction -> tubules not absorbing much; sodium and urea builds up in bladder -> pulls water out. Give IV fluids after post-obstructive diuresis.
How does postrenal AKI change starling’sIncreased capsular hydrostatic pressure; decreased GFR.
If obstruction is higher than bladderPercutaenous nephrostomy tube.

Lecture 23 CKD

Question Answer
CKD definitionwhereas AKI is recent/ within month, CKD is > 3 months, irrespective of diagnosis AND OR kidney damage (abnormal pathology, imaging studies or urinanalysis). GFR <60**** Ml/min.
Azotemia vs UremiaAzotemia refers strictly to elevation in BUN and Cr (seen in both CKD and AKI) vs. Uremia are specifically symptoms of renal failure, usually when BUN down to 20 or less.
Uremia FUN CAMPFatigue, Uremic Acidosis, Nausea/ vomiting, CNS (mental status changes), Appetite (decreased), Metallic taste in mouth, Pruritus/ itching.
CKD from glomerular diseases will haveEdema, proteinuria, RBC casts.
CKD from vascular diseasesHTN.
CKD from tubulointerstitial diseasesPolyuria, acidosis, hyper or hypokalemia. Not due to reduced GFR but from tubule dysfunction.
Kidney disease clinical signsHTN, edema, change in urinary composition or volume and Uremia.
Reduced renal function always indicated byreduced GFR.
Kidney damage determined viaUrinalysis (proteinuria, hematuria, polyuria) and or renal ultrasound.
Why is Cr imperfectSome secreted and also tied to muscle mass because it is the end metabolic product of muscle-derived Cr and phosphocreatine.
Serum creatinine will be higher whenCr secretion is inhibited by Cimetidine, Trimethoprim and or Dapsone. So, less secretion, slightly higher.
Stages of CKD, which is worst5. <15 GFR. Dialysis. Recall, anything less than 60 is significant.
HTN in CKD is fromNa surfeit. Edema won’t happen until GFR is below 10 ml/min.
When GFR<10 in CKDEdema and hyponatremia from inability to concentrate or dilute urine; water excretion < intake. Oliguric. Also Hyperkalemia. HTN. Uremic Acidosis.
Secondary HyperPTHDecreased renal production of 1, 25 Vit D reduced Ca + Phosphate retention -> PTH increases -> Hypocalcemia and High P**.
Clinical consequences of secondary hyperparathyroidismMetabolic bone disease and dystrophic calcification (dystrophic -> dead tissue -> nidus for Ca deposit).
CKD -> death fromCVD.

Lecture 24, 25

Question Answer
Uremic pericarditisAcute hemodialysis. Risk for bleed, tamponade.
Indications for acute hemodialysis secondary to uremiaUremic pericarditis, seizures, uncontrollable bleeding (-> PLT dysfunction).
Diabetic nephropathy is only seen in Type 2 DMWRONG. Both. But Type 2 more commonly leads to nephropathy but type 1 has more prominent symptoms.
Diabetic nephropathy occurs how many years after dx of DM? vs proteinuria?Rarely before 5 years, peaks at 15 years and 1-2 years after proteinuria.
#1 cause of kidney failure? #2?DM. HTN is #2.
DM -> Nephropathy either by advanced glycosylation endproducts (hyperglycemia related accumulations) and or systemic HTN and or intraglomerular HTN with A2 mediated efferent vasoconstriction.
Question Answer
First sign of Diabetic nephropathy?Microalbuminuria (30-300 mg/day). May coexist with hyperfiltration/ higher GFR than normal.
DNephropathy on pathMesangial expansion; thickened BM; nodular glomerular sclerosis called Kimmelstein-Wilson nodules
Albuminuria test of use>30 Albumin/ g creatinine on 2 of 3 random urine specimens. Vs. just testing albuminuria per day.